Consideration of additional human polymorphisms of interest including those regulating expression of endothelial receptors such as CD36 and endothelial protein C receptor [54], and those regulating the inflammatory response, including complement receptor 1, nitric oxide synthase 2, and tumor necrosis factor-α[55] will enable a fuller understanding of the impact of human genetics on risks of uncomplicated and severe malaria. This evidence concerns the gene NOS2 and malaria.